The Pathophysiological Basis of Parkinson’s Disease
The Pathophysiological Basis of Parkinson’s Disease
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Original abstract
Parkinson’s syndrome, or parkinsonism, involving the clinical symptoms first described in 1817 by James Parkinson 1, occurs in a variety of disorders of the central nervous system (CNS), and is basically characterized by dysfunction of the dopaminergic nigro-striatal system. It may, or in rare cases it may not, be associated with distinct anatomical damage to melanin-containing neurons of the substantia nigra (SN), changes in the neuronal cytoskeleton including the presence of Lewy bodies, and pathological changes in other neuronal systems, often as part of a more widespread process 2. The term Parkinson’s disease (PD) is properly restricted to paralysis agitans, the idiopathic form of parkinsonism, associated with the formation of Lewy bodies and the loss of neurons in the pars compacta of the SN (SNC), which has been known since the time of Tretiakoff 3 as the system principally at risk in this disorder. It can be accompanied by nonspecific or age-related brain pathology, and a variety of other coincidental lesions elsewhere in the CNS.